NU 665D Exam 3
1. New Anticoagulants: -3 currently approved
-Tested against coumadin
-No sign. diff b/w the three of them except for S/Es
-Avoid potent Pgp inducers (rifampin, carbemazepine, phehytoin, phenobarb, St.John's wort)
as will decrease effect
-Riva and Apixa: Avoid potent inhibitors of CYP3A4 and Pgp (Azoles, Proteaseinhibitors,
mycins), as will INCREASE AC effect
2. Eliquis (apixaban): Dose: 5mg BID
Renal adjustment: 2.5mg twice daily, must have 2 or more of the following: Age
>80yo, Body wt </= 60kg, Serum creatinine >/= 1.5mg/dLHalf life: 12 hours
Time to Peak: 3-4hoursDirect factor Xa inhibitor
3. Xarelto (rivaroxaban): Dose: 20mg daily w/evening meal of at least 500 caloriesfor
absorption
Renal Adjustment: CrCl 15-50mg once daily w/evening meal; CrCl <15mL/min: avoiduse
Half life: 5-13 hoursPeak: 2-4 hours
Director Factor Xa inhibitor
4. Pradaxa (dabigatran): Dose: 150mg BID
Renal adjustment: 75mg BID; not adequately studied
>10% pts have GI distress
Half life: 12-17hours, Up to 28hours w/renal impairmentPeak: 1-2hours
Direct thrombin inhibitor
5. Coumadin: -Obtain baseline PT/INR and investigate if abnormal
-Determine use of potential warfarin interactions (meds)
-Document target INR and RX warfarin tablet strength
-Provide pt edu on safety, monitoring, food and drug interactions
-Recommend 1st INR check on day 3-4
6. Coumadin Initiation: Day 1-3, initial dose: 5mg (10mg)Day 3-4:
-1.0-1.3 Dose 7.5mg
-1.4-1.5 Dose 5mg
,-1.6-1.8 Dose 5/2.5mg alternating dose
->1.0 Dose 2.5mg
->2.0 hold x1 day, then 2.5mg
Reversal agents: Vitamin K 1-10mg IV/PO (not SQ/IM); Takes 6 (IV) to 25 (PO) hoursto reverse
warfarin
7. Treatment Approach for A.Fib: 3 Elements:
1) Rate control
2) Restoration and maintenance of sinus rhythm (if indicated)
3) Stroke prevention
-Goal is to alleviate sxs and improve QOL
8. Rhythm Control: Focus on restoration of sinus rhythm:
-Palpitations
-SOB
-Dizziness/Lightheadedness
-Activity intolerance
Prevention of tachycardia-induced cardiomyopathyPrevention of hemodynamic compromise
r/t A.Fib
9. Rhythm Control Treatment: Specific tx type depends on several factors:
-Heart disease w/LVH or depressed LVEF
-HF
-Age
-Underlying sinus node dysfunction
-Other arrhythmias (e.g. a. flutter)
-Underlying QT prolongation
-Renal function
Note: pts w/a CHADS2VASc2 score of zero who opt for a rhythm control strategymay be
considered to stop OAC
10. Pharmacologic Management of A. Fib: Class 1: Na+ channel blockers, Quini-dine,
Procainamide, Disopyramide, Lidocaine, Mexilitine, Flecainide, PropafenoneClass 2: Beta
Blockers
Class 3: K+ channel blockers, Sotalol, Amiodarone, Dofetilide, Dronedarone
11. Side Effects of A. Fib Drugs: -Amiodarone Toxicity: pulmonary, thyroid, liver,
photosensitivity, skin discoloration
,-QT Prolongation
-Avoid QT prolonging meds
12. Ablation Procedure: -Pulmonary vein Isolation (LA)
-Radiofreq. ablation
-Not curative, but sign. reduces the amount of A. Fib
-General anesthesia, groin access
-Generally reserved for pts who have failed at least one attempt at DC cardioversion,1 or 2
antiarrhythmic agents
13. Rate Control: General goal: 60-80 BPM at restNot all pts req drug therapy for this
Tx with: BB (metoprolol, atenolol, carvidolol (HF), Non-dihydropyridine CCB (dilti-azem,
verapamil), Digoxin (not 1st line)
Consider co-morbidities: HF (non-dihydropyrodine CCB should not be used in HFwith low
EF d/t negative ionotropic effect; LVEF
-Rate control strategy can be appropriate for older pts who are more prone to druginteractions
and are asymptomic in A.Fib
14. Heart Failure: Inability of the heart to provide forward output to meet the perfu-sion and
oxygenation requirements while maintaining normal filling pressures
15. Systolic Dysfunction: Impaired cardiac contractile function
-Majority of heart failure cases
-Left or right sided
-Abnormalities in the systolic function
-Reduced LVEF often <50%
-Progressive chamber dilation
16. Diastolic Dysfunction: Abnormal cardiac relaxation, stiffness or filling
-Normal LVEF
-Often dx'd when pts present w/HF sxs and preserved LVEF
-Often hypertrophic w/impaired relaxtion
-Longstanind uncontrolled HTN
17. Left Sided HF: -Often presents w/pulmonary edema, fluid backing up in pul-monary
circuit
-Decreased contracility and cardiac output
-Compensatory increase in catecholamines to drive up cardiac output
, -Catecholamin increase causes increased BP
-Laterally displaced apical pulse
-S3 Gallop rhythm
18. P Wave: Atrial depolarization
19. P-R Interval: 0.12-0.20 seconds
20. QRS Complex: Ventricular Depolarization0.06-0.10 (up to 0.12) seconds
21. ST Segment: Beginning of repolarization; should be isoelectric
22. T Wave: End of ventricular depolarization
23. QT Interval: Ventricular repolarizationMen <0.44 seconds
Women < (or = to) 0.46 seconds
24. Depolarization: Wave of positively charged sodium ions passing through themyocardium
25. Repolarization: Returning to a polarized stateOccurs by potassium ions leaving the cells
26. Electricity of heart: In RA starting at SA node, moving through heart, slowing (d/tCa++
ions), pass thru AV node
Conducts rapidly (Na+ ions), through the bundle of His, down through right and leftbundle
branches
27. Atrial Fibrillation: Irregularly irregular rhythm
-Absence of discernible P wave
-Atrial disorganization
28. Paroxysmal A. Fib: -Recurrent
>1 episode lasting 30 or more seconds in durationAF that terminates spontaneously within 7
days
29. Persistent A. Fib: Sustained A. Fib >7 days ORLasts <7 days but requires cardioversion
30. Permanent A. Fib: Refractory to cardioversion or accepted as a final rhythm
31. Acute A. Fib: New onset OR first episode of A. Fib
32. Lone A. Fib: patients <60yo without evidence of cardiac, pulmonary or circula-tory
disease
33. A. Fib Associated Cardiac Conditions: -HTN
-CHF
-CAD
-Rheumatic valvular disease
1. New Anticoagulants: -3 currently approved
-Tested against coumadin
-No sign. diff b/w the three of them except for S/Es
-Avoid potent Pgp inducers (rifampin, carbemazepine, phehytoin, phenobarb, St.John's wort)
as will decrease effect
-Riva and Apixa: Avoid potent inhibitors of CYP3A4 and Pgp (Azoles, Proteaseinhibitors,
mycins), as will INCREASE AC effect
2. Eliquis (apixaban): Dose: 5mg BID
Renal adjustment: 2.5mg twice daily, must have 2 or more of the following: Age
>80yo, Body wt </= 60kg, Serum creatinine >/= 1.5mg/dLHalf life: 12 hours
Time to Peak: 3-4hoursDirect factor Xa inhibitor
3. Xarelto (rivaroxaban): Dose: 20mg daily w/evening meal of at least 500 caloriesfor
absorption
Renal Adjustment: CrCl 15-50mg once daily w/evening meal; CrCl <15mL/min: avoiduse
Half life: 5-13 hoursPeak: 2-4 hours
Director Factor Xa inhibitor
4. Pradaxa (dabigatran): Dose: 150mg BID
Renal adjustment: 75mg BID; not adequately studied
>10% pts have GI distress
Half life: 12-17hours, Up to 28hours w/renal impairmentPeak: 1-2hours
Direct thrombin inhibitor
5. Coumadin: -Obtain baseline PT/INR and investigate if abnormal
-Determine use of potential warfarin interactions (meds)
-Document target INR and RX warfarin tablet strength
-Provide pt edu on safety, monitoring, food and drug interactions
-Recommend 1st INR check on day 3-4
6. Coumadin Initiation: Day 1-3, initial dose: 5mg (10mg)Day 3-4:
-1.0-1.3 Dose 7.5mg
-1.4-1.5 Dose 5mg
,-1.6-1.8 Dose 5/2.5mg alternating dose
->1.0 Dose 2.5mg
->2.0 hold x1 day, then 2.5mg
Reversal agents: Vitamin K 1-10mg IV/PO (not SQ/IM); Takes 6 (IV) to 25 (PO) hoursto reverse
warfarin
7. Treatment Approach for A.Fib: 3 Elements:
1) Rate control
2) Restoration and maintenance of sinus rhythm (if indicated)
3) Stroke prevention
-Goal is to alleviate sxs and improve QOL
8. Rhythm Control: Focus on restoration of sinus rhythm:
-Palpitations
-SOB
-Dizziness/Lightheadedness
-Activity intolerance
Prevention of tachycardia-induced cardiomyopathyPrevention of hemodynamic compromise
r/t A.Fib
9. Rhythm Control Treatment: Specific tx type depends on several factors:
-Heart disease w/LVH or depressed LVEF
-HF
-Age
-Underlying sinus node dysfunction
-Other arrhythmias (e.g. a. flutter)
-Underlying QT prolongation
-Renal function
Note: pts w/a CHADS2VASc2 score of zero who opt for a rhythm control strategymay be
considered to stop OAC
10. Pharmacologic Management of A. Fib: Class 1: Na+ channel blockers, Quini-dine,
Procainamide, Disopyramide, Lidocaine, Mexilitine, Flecainide, PropafenoneClass 2: Beta
Blockers
Class 3: K+ channel blockers, Sotalol, Amiodarone, Dofetilide, Dronedarone
11. Side Effects of A. Fib Drugs: -Amiodarone Toxicity: pulmonary, thyroid, liver,
photosensitivity, skin discoloration
,-QT Prolongation
-Avoid QT prolonging meds
12. Ablation Procedure: -Pulmonary vein Isolation (LA)
-Radiofreq. ablation
-Not curative, but sign. reduces the amount of A. Fib
-General anesthesia, groin access
-Generally reserved for pts who have failed at least one attempt at DC cardioversion,1 or 2
antiarrhythmic agents
13. Rate Control: General goal: 60-80 BPM at restNot all pts req drug therapy for this
Tx with: BB (metoprolol, atenolol, carvidolol (HF), Non-dihydropyridine CCB (dilti-azem,
verapamil), Digoxin (not 1st line)
Consider co-morbidities: HF (non-dihydropyrodine CCB should not be used in HFwith low
EF d/t negative ionotropic effect; LVEF
-Rate control strategy can be appropriate for older pts who are more prone to druginteractions
and are asymptomic in A.Fib
14. Heart Failure: Inability of the heart to provide forward output to meet the perfu-sion and
oxygenation requirements while maintaining normal filling pressures
15. Systolic Dysfunction: Impaired cardiac contractile function
-Majority of heart failure cases
-Left or right sided
-Abnormalities in the systolic function
-Reduced LVEF often <50%
-Progressive chamber dilation
16. Diastolic Dysfunction: Abnormal cardiac relaxation, stiffness or filling
-Normal LVEF
-Often dx'd when pts present w/HF sxs and preserved LVEF
-Often hypertrophic w/impaired relaxtion
-Longstanind uncontrolled HTN
17. Left Sided HF: -Often presents w/pulmonary edema, fluid backing up in pul-monary
circuit
-Decreased contracility and cardiac output
-Compensatory increase in catecholamines to drive up cardiac output
, -Catecholamin increase causes increased BP
-Laterally displaced apical pulse
-S3 Gallop rhythm
18. P Wave: Atrial depolarization
19. P-R Interval: 0.12-0.20 seconds
20. QRS Complex: Ventricular Depolarization0.06-0.10 (up to 0.12) seconds
21. ST Segment: Beginning of repolarization; should be isoelectric
22. T Wave: End of ventricular depolarization
23. QT Interval: Ventricular repolarizationMen <0.44 seconds
Women < (or = to) 0.46 seconds
24. Depolarization: Wave of positively charged sodium ions passing through themyocardium
25. Repolarization: Returning to a polarized stateOccurs by potassium ions leaving the cells
26. Electricity of heart: In RA starting at SA node, moving through heart, slowing (d/tCa++
ions), pass thru AV node
Conducts rapidly (Na+ ions), through the bundle of His, down through right and leftbundle
branches
27. Atrial Fibrillation: Irregularly irregular rhythm
-Absence of discernible P wave
-Atrial disorganization
28. Paroxysmal A. Fib: -Recurrent
>1 episode lasting 30 or more seconds in durationAF that terminates spontaneously within 7
days
29. Persistent A. Fib: Sustained A. Fib >7 days ORLasts <7 days but requires cardioversion
30. Permanent A. Fib: Refractory to cardioversion or accepted as a final rhythm
31. Acute A. Fib: New onset OR first episode of A. Fib
32. Lone A. Fib: patients <60yo without evidence of cardiac, pulmonary or circula-tory
disease
33. A. Fib Associated Cardiac Conditions: -HTN
-CHF
-CAD
-Rheumatic valvular disease
